5 years.
Not applicable.
Microcrystalline cellulose (E460)
Calcium hydrogen phosphate, anhydrous
Maize starch
Polacrilin potassium
Povidone (polyvidone)
Glycerol 85%
Magnesium stearate
Meglumine
Poloxamer
Iron oxide, yellow (1 mg tablets only) (E172)
Iron oxide, red (2 mg tablets only) (E172)
Non-clinical data revealed no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity and carcinogenic potential.
Repaglinide was shown not to be teratogenic in animal studies. Embryotoxicity, abnormal limb development in rat foetuses and new born pups, was observed in female rats exposed to high doses in the last stage of pregnancy and during the lactation period. Repaglinide was detected in the milk of animals.
Absorption
Repaglinide is rapidly absorbed from the gastrointestinal tract, which leads to a rapid increase in the plasma concentration of the active substance. The peak plasma level occurs within one hour post administration. After reaching a maximum, the plasma level decreases rapidly.
Repaglinide pharmacokinetics are characterised by a mean absolute bioavailability of 63% (CV 11%).
No clinically relevant differences were seen in the pharmacokinetics of repaglinide, when repaglinide was administered 0, 15 or 30 minutes before a meal or in fasting state.
A high interindividual variability (60%) in repaglinide plasma concentrations has been detected in the clinical trials. Intraindividual variability is low to moderate (35%) and as repaglinide should be titrated against the clinical response, efficacy is not affected by interindividual variability.
Distribution
Repaglinide pharmacokinetics are characterised by low volume of distribution, 30 L (consistent with distribution into intracellular fluid) and is highly bound to plasma proteins in humans (greater than 98%).
Elimination
Repaglinide is eliminated rapidly within 4 - 6 hours from the blood. The plasma elimination half-life is approximately one hour.
Repaglinide is almost completely metabolised, and no metabolites with clinically relevant hypoglycaemic effect have been identified.
Repaglinide metabolites are excreted primarily via the bile. A small fraction (less than 8%) of the administered dose appears in the urine, primarily as metabolites. Less than 1% of repaglinide is recovered in faeces.
Special patient groups
Repaglinide exposure is increased in patients with hepatic insufficiency and in the elderly type 2 diabetic patients. The AUC (SD) after 2 mg single dose exposure (4 mg in patients with hepatic insufficiency) was 31.4 ng/ml x hr (28.3) in healthy volunteers, 304.9 ng/ml x hr (228.0) in patients with hepatic insufficiency, and 117.9 ng/ml x hr (83.8) in the elderly type 2 diabetic patients.
After a 5 day treatment of repaglinide (2 mg x 3/day) in patients with a severe impaired renal function (creatinine clearance: 20-39 ml/min.), the results showed a significant 2-fold increase of the exposure (AUC) and half-life (t1/2) as compared to patients with normal renal function.
Paediatric population
No data are available.
05/2016
Novo Nordisk A/S
Novo Allé
DK-2880 Bagsværd
Denmark
Store in the original package in order to protect from moisture.
The blister pack (aluminium/aluminium) contains 30, 90, 120 or 270 tablets, respectively.
Not all pack sizes may be marketed.
Prandin 0.5 mg | EU/1/00/162/003-005, EU/1/00/162/021 |
Prandin 1 mg | EU/1/00/162/009-011, EU/1/00/162/020 |
Prandin 2 mg | EU/1/00/162/015-017, EU/1/00/162/019 |
No special requirements.
Date of first authorisation: 29 January 2001
Date of last renewal: 23 July 2008
